scholarly journals The developmental impact of prenatal stress, prenatal dexamethasone and postnatal social stress on physiology, behaviour and neuroanatomy of primate offspring: studies in rhesus macaque and common marmoset

2010 ◽  
Vol 214 (1) ◽  
pp. 33-53 ◽  
Author(s):  
Christopher R. Pryce ◽  
Yves Aubert ◽  
Claudia Maier ◽  
Peter C. Pearce ◽  
Eberhard Fuchs
2019 ◽  
Author(s):  
H Scott ◽  
TJ Phillips ◽  
Y Sze ◽  
A Alfieri ◽  
MF Rogers ◽  
...  

AbstractMaternal exposure to social stress during pregnancy is associated with an increased risk of psychiatric disorders in the offspring in later life. However, the mechanism through which the effects of maternal stress are transmitted to the foetus is unclear. Using a rat model, we explored the mechanisms by which maternal social stress is conveyed to the foetus and the potential for targeted treatment to prevent disease in the offspring. Maternal stress increased circulating corticosterone in the mother, but not the foetuses. Maternal stress also induced oxidative stress in the placenta, but not in the foetal brain, and this was prevented by administration of a nanoparticle-bound antioxidant. Moreover, antioxidant treatment prevented prenatal stress-induced anxiety-like behaviour in the adult male offspring, along with several stress-induced neuroanatomical, neurochemical and gene expression changes in the offspring brain. Importantly, many of these neural effects were mimicked in neuronal cultures by application of placental-conditioned medium or foetal plasma from stressed pregnancies. Both placental-conditioned medium and foetal plasma contained differentially abundant extracellular microRNAs following prenatal stress. The present study highlights the crucial role of the placenta, and the molecules it secretes, in foetal brain development and provides evidence of the potential for treatment that can prevent maternal stress-induced foetal programming of neurological disease.


PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0172093 ◽  
Author(s):  
Pin Yu ◽  
Yanfeng Xu ◽  
Wei Deng ◽  
Linlin Bao ◽  
Lan Huang ◽  
...  

Reproduction ◽  
2013 ◽  
Vol 146 (5) ◽  
pp. R175-R189 ◽  
Author(s):  
Paula J Brunton

A suboptimalin uteroenvironment, for example, as a result of maternal stress, can have detrimental effects on the pregnancy and long-term adverse ‘programming’ effects on the offspring. This article focuses on the effects of prenatal social stress on the mother, her pregnancy and the offspring, since these issues have ethological relevance in both animals and humans. The consequences of social stress exposure depend on when during pregnancy the stress occurs, and many of the effects on the offspring are sex specific. Social stress during early pregnancy tends to result in pregnancy loss, whereas stress exposure later in pregnancy, when the mother has already invested considerable resources in the foetuses, results in programmed offspring of low birth weight: a risk factor for various adulthood diseases. Neuroendocrine and behavioural responses to stress in the offspring are particularly sensitive to foetal programming by prenatal stress, indicated by enhanced hypothalamo-pituitary–adrenal (HPA) axis responses and increased anxiety behaviour, which result from permanent changes in the offspring's brain. The dysregulation of HPA axis function may also interfere with other systems, for example, the hypothalamic–pituitary–gonadal axis, as there is evidence for alterations in steroidogenesis, reproductive potential and impaired reproductive/social behaviours in prenatally stressed offspring. Prenatal social stress also programmes future maternal behaviour, highlighting the potential for negative phenotypes to be transmitted to future generations. The possible mechanisms through which maternal stress during pregnancy is transmitted to the foetuses and the foetal brain is programmed by prenatal stress and the potential to overwrite programming of the offspring are discussed.


2013 ◽  
Vol 217 (2) ◽  
pp. 161-173 ◽  
Author(s):  
Paula J Brunton ◽  
Katie M Sullivan ◽  
David Kerrigan ◽  
John A Russell ◽  
Jonathan R Seckl ◽  
...  

Glucocorticoid overexposure during pregnancy programmes offspring physiology and predisposes to later disease. However, any impact of ethologically relevant maternal stress is less clear, yet of physiological importance. Here, we investigated in rats the short- and long-term effects in adult offspring of repeated social stress (exposure to an aggressive lactating female) during late pregnancy on glucose regulation following stress, glucose–insulin homoeostasis and peripheral expression of genes important in regulating glucose and lipid metabolism and glucocorticoid action. Prenatal stress (PNS) was associated with reduced birth weight in female, but not male, offspring. The increase in blood glucose with restraint was exaggerated in adult PNS males compared with controls, but not in females. Oral glucose tolerance testing showed no effects on plasma glucose or insulin concentrations in either sex at 3 months; however, at 6 months, PNS females were hyperinsulinaemic following an oral glucose load. In PNS males, plasma triglyceride concentrations were increased, with reduced hepatic mRNA expression of 5α-reductase and peroxisome proliferator-activated receptor α (Pparα(Ppara)) and a strong trend towards reduced peroxisome proliferator-activated receptor gamma coactivator 1α (Pgc1α(Ppargc1a)) andPparγ(Pparg) expression, whereas onlyPgc1αmRNA was affected in PNS females. Conversely, in subcutaneous fat, PNS reduced mRNA expression of 11β-hydroxysteroid dehydrogenase type 1 (11βhsd1), phosphoenolpyruvate carboxykinase (Pepck(Pck1)), adipose triglyceride lipase (Atgl) and diglyceride acyltransferase 2 (Dgat2) in females, but onlyPepckmRNA expression was reduced in PNS males. Thus, prenatal social stress differentially programmes glucose homoeostasis and peripheral metabolism in male and female offspring. These long-term alterations in physiology may increase susceptibility to metabolic disease.


2020 ◽  
Vol 68 (4) ◽  
pp. 217-227 ◽  
Author(s):  
Lisanne J. Bulling ◽  
Isabella C. Bertschi ◽  
Céline C. Stadelmann ◽  
Tina Niederer ◽  
Guy Bodenmann

Zusammenfassung. Die vorliegende Arbeit stellt die bisherigen empirischen Befunde zur Sprachgrundfrequenz (f0) in Paargesprächen vor und untersucht, wie sich die f0 nach einer experimentellen Stressinduktion im anschließenden spontanen Gespräch zwischen den Partner_innen verändert, wie die f0 mit der verbalen Stressäußerung zusammenhängt und wie sie zwischen den beiden Partner_innen kovariiert. Von 128 heterosexuellen Paaren nahm jeweils eine Person pro Paar am Trier Social Stress Test (TSST) teil. Die dem TSST vorangehende und anschließende naturalistische Interaktion zwischen den Partner_innen wurde gefilmt und nach Gesprächsthema und Art der Stressäußerung kodiert. Wie vorherige Studien zur f0 im Paargespräch zeigte auch die vorliegende Studie, dass die f0 wichtige Informationen über die Partnerschaft enthält. Während eine Erhöhung der f0 in Gesprächen über einen paarinternen Stressor (d.h. bei Konfliktgesprächen) mit negativen Kommunikationsmustern einherging, zeigte die vorliegende Studie, dass die f0 bei Gesprächen über einen paarexternen Stressor (d.h. beim TSST) mit emotionsorientierten Stressäußerungen einherging, also einer für den Stressbewältigungsprozess förderlichen Art der Kommunikation. Die Oszillatorenmodelle zeigen darüber hinaus, dass eine Kopplung der f0 zwischen den Partner_innen besteht, was darauf hindeutet, dass die nicht gestressten Partner_innen auf die paraverbalen Stressäußerungen der gestressten Partner_innen mit ihren eigenen paraverbalen Stressäußerungen reagieren.


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